Canadian Journal of Anesthesia, Vol 27, 146-149, Copyright © 1980 by Canadian Anesthesiologists' Society

Effects of Prostaglandins and Indomethacin on Neuromuscular Blocking Agents

¹ Department of Anesthesiology, University of Utah College of Medicine, 50 North Medical Drive, Salt Lake City, Utah, 84132, U.S.A.; Saint Vincent Hospital, Billings, Montana
² Department of Anesthesiology, University of Utah College of Medicine, 50 North Medical Drive, Salt Lake City, Utah, 84132, U.S.A.

The effects on neuromuscular blockade by d-tubocurarine and succinylcholine of inhibition prostaglandin biosynthesis by indomethacin and of intra-arterial administration of prostoglandins E₂ and F_{2 alpha}, before and after inhibition of prostoglandin biosynthesis, were evaluated in the cat sciatic-tibialis preparation.

Non-specific inhibition of prostaglandin biosynthesis by indomethacin 3 mg·kg^-1 did not alter latency, maximal blockade or duration of neuromuscular blockade induced by d-tubocurarine or succinylcholine.

Prostaglandin E₂ antagonized twitch height depression by d-tubocurarine by an average of six per cent before and by 15 per cent after indomethacin, but potentiated the neuromuscular block of succinylcholine by an average of five per cent before and 60 per cent after indomethacin. Prostaglandin F_{2 alpha} antagonized d-tubocurarine neuromuscular block by an average of 10 per cent before and 18 per cent after indomethacin, but potentiated succinylcholine block by an average of four per cent before and 12 per cent after indomethacin.

These results suggest that non-specific inhibition of prostaglandin biosynthesis alone does not influence d-tubocurarine or succinylcholine induced neuromuscular blockades. However, both prostaglandin E₂ and F_{2 alpha} may induce transmitter release at the neuromuscular junction that may be enhanced by indomethacin, thus antagonizing the non-depolarizing blockade of d-tubocurarine and potentiating the depolarizing blockade of succinylcholine.